Blood stasis is one of the main pathogenesis of geriatrics.The main traits of geriatrics blood stasis are: blood stasis mainly induced by def iciency,def iciency and stasis is concomitant,stasis builds up gradually,symptoms of blood stasis aren’t mandatory in clinic practice,the range and severity of blood stasis is so wide and severe that it’s hard to be dissipated.Activating circulation to dissipate stasis is followed through the whole therapeutic process,and often used with replenishing qi,invigorating the kidney,and nourishing blood in order to dissipate stasis without hurting vital qi as well as reinforcing vital energy to dissipate stasis.

BACKGROUND:In recent years, with the use of new immunosuppressive agents, the survival rate of renal graft is greatly improved, but accompanied by lots of side effects and unchanged long-term graft survival. Mesenchymal stem cel s (MSCs) have aroused people’s great interest, while their efficacy in kidney transplantation remains controversial.
OBJECTIVE:To evaluate the efficacy of MSCs transplantation on post-transplant renal graft function with a systematic review.
METHODS:PubMed, EMBASE, the Cochrane Library database, the Cochrane Central Register of Control ed Trials, Wanfang database and China National Knowledge Infrastructure (CNKI) were searched until November 2015. Revman 5.3 was used for statistical analysis.
RESULTS AND CONCLUSION:A total of 6 randomized control ed trials were included, including 1 166 patients. Meta-analysis results showed that at 1, 2 weeks and 1 month after kidney transplantation, the posttransplantation estimated glomerular filtration rates in the MSC-treated group were significantly higher than those in the control group (P<0.05). At 1, 3, 6, 12 months after kidney transplantation, the posttransplantation serum creatinine levels showed no significant difference between the MSC-treated group and the control group (P>0.05). To conclude, MSC-based immunosuppression regimen is superior to current standard immunotherapy in improving renal graft function in the early stage after kidney transplantation, but the clinical efficacy is diminished in the later period. Therefore, further investigation using large-scale randomized control ed trials is warranted.

BackgroundMental health issues have become increasingly prominent amid rising societal pressure. Depressive disorders， characterized as chronic and recurrent conditions， adversely affect patients' physical and mental well-being while imposing a significant economic burden. Previous studies on depressive disorders in China have relied on cross-sectional surveys， capturing prevalence at specific time points， but lacking systematic analyses across age， period， and cohort dimensions. ObjectiveTo analyze long-term trends in the disease burden of depressive disorder in the Chinese population from 1990 to 2021， and to provide references to inform prevention and treatment strategies. MethodsData on the disease burden of depressive disorders in China were obtained from the Global Burden of Disease Study 2021 （GBD 2021） database. A joinpoint regression model was used to analyze trends in the disease burden. An age-period-cohort model， implemented in Stata 17.0， was applied to assess variations in incidence and disease burden attributable to age， period and cohort effects. ResultsFrom 1990 to 2021， the disability-adjusted life year （DALY） rate for depressive disorders in China decreased by an average of 0.27% annually， while the incidence rate decreased by an average of 0.24% annually. Females had higher incidence and DALY rates than those of males. The age-period-cohort model analysis revealed that age effects on incidence and disease burden steadily increased， period effects declined over time， and cohort effects initially increased and then declined. ConclusionFrom 1990 to 2021， both the incidence and DALY rates of depressive disorders in China showed a declining trend. Females experienced a higher burden compare to males. Additionally， incidence and DALY rates increased with age but declined over time.

OBJECTIVE To detect potential mutations of the EXT1 and EXT2 genes in a pedigree affected with hereditary multiple exostosis (HME). METHODS For a four-generation family with 7 affected individuals from 17 family members,genomic DNA was extracted from peripheral venous blood samples. All exons of the EXT1 and EXT2 genes were screened for potential mutation by PCR and Sanger sequencing. RESULTS A novel heterozygous frameshift mutation c.1202delT (p.I401Tfs*2)was found in exon 4 of the EXT1 gene in the proband and the other 6 affected individuals. The same mutation was not detected among the healthy members from the family. The mutation has given rise a truncated EXT1 protein with loss of 345 amino acids. CONCLUSION A novel frameshift mutation of the EXT1 gene has been identified in a pedigree affected with HME, which has enriched the mutational spectrum of the EXT1 gene and may facilitate genetic counseling and prenatal diagnosis for the family.

OBJECTIVETo detect potential mutation of the WAS gene in a Chinese family affected with Wiskott-Aldrich syndrome.

METHODSPeripheral blood samples were collected from the proband and his family members. All exons and flanking regions of the WAS gene were subjected to PCR amplification - Sanger sequencing as well as restriction endonuclease analysis. Plasma level of B-cell activating factor (BAFF) was also determined for all family members.

RESULTSA hemizygous mutation (c.257G>A) of the WAS gene was identified in all patients from the family, for which the patient's mother was heterozygous. The same mutation was not found among healthy members of the family. Compared with unaffected members, all patients had a higher level of BAFF.

CONCLUSIONThe c.257G>A mutation of the WAS gene probably underlies the Wiskott-Aldrich syndrome in this family.

B-Cell Activating Factor ; blood ; Child, Preschool ; Heterozygote ; Humans ; Male ; Mutation ; Wiskott-Aldrich Syndrome ; genetics ; Wiskott-Aldrich Syndrome Protein ; genetics

Objective To study the effect of using different tibial nerve proximal muscle branchs to repair deep peroneal nerve injury in animal experiment, and to screen out the most optimal donor nerve branch. Methods From June, 2016 to August, 2016, 64 adult female SD rats were randomly divided into 4 groups, which were LHG (using lateral head of gastrocnemius to repair peroneal nerve), MHG(using medial head of gastrocnemius to repair peroneal nerve), SNB (using soleus nerve branch to repair peroneal nerve), and blank. There were16 rats in each group. At 4 and 8 weeks after surgery, each group were tested on behavior, electrophysiology, muscle tension, muscle wet weight and histology, to evaluate function recovery of the muscles controlled by deep peroneal nerve in each group, and to compare recovery of the deep peroneal nerve repaired by different tibial nerve branches. Results Eight weeks after surgery,right foot of the rats in LHG,MHG and SNB group can be extended,toes can be completely opened. Rats in blank group showed limping gait, whose right foot can not be extended, right toe can not be opened, and muscle atrophied. At 4 and 8 weeks after the operation, the recovery rate of LHG, MHG, SNB group (at 4th weeks, 33.60 ±2.22)%, 33.07 ±2.38% and 35.91 ±2.02%; at 8th weeks, 67.16 ±5.74)%, 66.56 ±3.18% and 73.17 ± 5.33%, respectively)was higher than blank group(7.71±1.05% and 7.84±0.78%, respectively)on CMAP amplitude, tibialis anterior muscle contractility, tibialis anterior muscle cell area, muscle cell area. SNB group was superior to the LHG group and LHG group.And the difference was statistically significant(P<0.05). Conclusion All the proxi-mal tibial nerve muscle branchs can be used to repair the deep peroneal nerve injury, and the soleus nerve branch is the preferred donor nerve.

OBJECTIVE: To explore the genetic basis for a Chinese pedigree affected with dyschromatosis symmetrica hereditaria (DSH). METHODS: PCR and Sanger sequencing were carried out for the proband, and suspected variant was validated by Sanger sequencing in the pedigree. RESULTS: The proband was found to harbor a novel variant of c.1352delA (p.N451Mfs*13) of the ADAR (NM_001111) gene. The same variant was found in her affected mother and sister, but not in her unaffected father, uncle, and 100 healthy individual. CONCLUSION The novel variant of the ADAR gene probably underlay the pathogenesis of DSH in this pedigree.
Adenosine Deaminase/genetics* ; China ; Female ; Humans ; Mutation ; Pedigree ; Pigmentation Disorders/congenital* ; RNA-Binding Proteins/genetics*

Objective:To establish and identify a SD rat model with reconstruction of bladder sensory and motor innervation , so as to lay the foundation for further study of micturition center remodeling and its mechanisms .Methods:A total of 45 female SD rats were randomly divided into control group(n=10) ,rhizotomy group(n=15) and nerve root anastomosis group(n=20) . All the ventral and dorsal roots of spinal nerve below L4 level of rats in rhizotomy group were cut off .In nerve root anastomosis group ,the bilateral ventral and dorsal roots of L4 nerve ,were anastomosed with those of S1 nerve ,after the spinal nerve roots had been cut off .Rats in control group were not treated with surgery . At Six months after surgery ,rats in each group underwent urodynamic test ,nerve root stimulation ,toluidine blue staining at nerve anastomosis site ,pelvic ganglia fluorescence gold tracer staining and bladder wet weight measurements .Results:Bladder maximum capacity ,residual urine volume ,bladder compliance and bladder wet weight in nerve root anastomosis group was less than those in rhizotomy group ,however ,larger than those in control group(P<0 .05) .There was no statistically significant difference in maximum voiding pressure between nerve root anastomosis group and control group(P> 0 .05) ,however ,maximum voiding pressure in nerve root anastomosis group was larger than that in rhizotomy group(P<0 .05) .Intravesical pressure increased after nerve root stimulation in nerve root anastomosis group ,but it was still lower than that in control group(P<0 .05) .Nerve passing rate was (53 .4 ± 6 .7)% in nerve root anastomosis group ,under toluidine blue staining at nerve anastomosis site .After injection of fluorescent gold in pelvic ganglia ,fluorescence gold staining was visible in the L4 spinal cord gray matter in nerve root anastomosis group , however ,not visible in rhizotomy group and control group .Conclusions:SD rat model with reconstruction of bladder sensory and motor innervation is successfully established .It lays the foundation for further study of micturition center remodeling and its mechanism .

OBJECTIVE: To explore the genetic basis for a pedigree affected with hereditary spastic paraplegia type 4 (HSP4). METHODS: Peripheral venous blood samples were taken from members of the four-generation pedigree and 50 healthy controls for the extraction of genomic DNA. Genes associated with peripheral neuropathy and hereditary spastic paraplegia were captured and subjected to targeted capture and next-generation sequencing. The results were confirmed by Sanger sequencing. RESULTS: DNA sequencing suggested that the proband has carried a heterozygous c.1196C>G variant in exon 9 of the SPAST gene, which can cause substitution of serine by threonine at position 399 (p.Ser399Trp) and lead to change in the protein function. The same variant was also detected in other patients from the pedigree but not among unaffected individuals or the 50 healthy controls. Based on the ACMG 2015 guidelines, the variant was predicted to be possibly pathogenic. CONCLUSION The c.1196C>G variant of the SPAST gene probably underlay the HSP4 in this pedigree.
Base Sequence ; Humans ; Mutation ; Paraplegia/genetics* ; Pedigree ; Sequence Analysis, DNA ; Spastic Paraplegia, Hereditary/genetics* ; Spastin/genetics*

Objective:To provide experimental evidence for genetic counseling and prenatal diagnosis by analyzing the clinical characteristics, screening and identification of the function of suspicious variants in a X-1inked spondyloepiphyseal dysplasia tarda (SEDT) family.Methods:The family members' medical history, general physical examination, femur, spine X-ray examination were collected. Peripheral blood samples of the family members were collected and DNA was extracted from these samples. Sequencing clinical whole exons of proband DNA by targeted gene high-throughput sequencing method, then analysis sequencing data. The suspicious mutation was confirmed in pedigree members by PCR and Sanger sequencing. Reverse transcription polymerase chain reaction (RT-PCR) experiments of total RNA from blood lymphocytes were performed. The amplification of exons 3 and 4 of the pathogenic gene were amplified and identified by agarose gel. The expression of the pathogenic gene was also detected.Results:Three affected males of the family were diagnosed with SEDT according to their clinical and radiological features. A nonsense mutation in the transport protein particle complex subunit 2 ( TRAPPC2) gene NM_001011658: c.91A>T (p.K31*) was found in the proband using whole exome sequencing. This variation was also detected in his cousin, but not in non-phenotypic members of the family. The RT-PCR result for amplification of exon 3 and 4 of peripheral blood lymphocytes was the same as those of normal controls, indicating that the mutation did not affect the splicing of transcripts. qPCR results showed that the transcriptional expression of TRAPPC2 in patients was significantly lower than that in family normal controls and normal people controls. Conclusion:Identification of the novel nonsense mutation (c.91A>T) in the SEDT family enables early patients screening, carrier detection, genetic counseling, prenatal diagnosis, and clinical prevention and treatment. The detailed genotype/phenotype descriptions contribute to the SEDT mutation spectrum. The study of the function of TRAPPC2 mutation will help to further elucidate the role of sedlin in cartilage.